eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic
Alcoholic Ketoacidosis: Treatment & Medication
Updated: Jul 28, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
- Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated.
- Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia.
- If the patient's mental status is diminished, consider administration of naloxone and thiamine.
- Note information about the patient's social situation and the presence of intoxicating agents besides alcohol.
Emergency Department Care
- Once the diagnosis of alcoholic ketoacidosis (AKA) is established, the mainstay of treatment is hydration with 5% dextrose in normal saline (D5 NS) to address the principal physiologic derangement, a lack of metabolic substrate (glucose).3 Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counter-regulatory hormones and by providing metabolic substrate. Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD+ ratio. Fluids alone do not correct AKA as quickly as fluids and carbohydrates together. Thiamine supplementation should also be given upon initiation of dextrose. Patients who can tolerate oral nutrition should be fed.
- In general, exogenous insulin is contraindicated in the treatment of AKA because it may cause life-threatening hypoglycemia in patients with depleted glycogen stores. In most cases, the patient's endogenous insulin levels rise appropriately with adequate carbohydrate and volume replacement. Insulin may be required in patients with diabetes who have AKA. If the patient's blood glucose level is significantly elevated, AKA may be indistinguishable from diabetic ketoacidosis (DKA). The disorders also may coexist.
- As rehydration progresses and adequate renal function is established, consider electrolyte replacement, giving particular attention to potassium and magnesium.
- If the anion gap fails to close as resuscitation continues, it is important to consider other causes of an anion gap acidosis such as methanol or ethylene glycol ingestion (co-ingestion). When considering other co-ingestants, note that alcoholic ketoacidosis can cause a mildly elevated osmolar gap (~20 mmol/kg).
- Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, seizures, or delirium. Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response.
- Bicarbonate therapy should only be considered in the face of severe life-threatening acidosis (ie, pH <7.1) that is unresponsive to fluid therapy.
- Associated disease states: Patients with alcoholic ketoacidosis (AKA) may have various coexisting illnesses, especially those commonly associated with chronic alcohol abuse. A thorough history and physical examination must be obtained. Associated conditions include pancreatitis, hepatitis, cirrhosis, coagulopathy, gastritis, GI bleeding, pneumonia, cardiomyopathy, alcohol withdrawal, infection, anemia, seizures, cerebrovascular accident (CVA), myopathy, rhabdomyolysis, neuropathy, arrhythmias, and intoxication with alcohol or other substances. These associated illnesses and conditions may be a significant source of morbidity and mortality if not properly addressed.
Medication
A requirement for any medication other than D5 NS is uncommon. Fluid resuscitation is the mainstay of treatment in alcoholic ketoacidosis (AKA).
The need to correct pH actively depends on the severity of the pH imbalance, the compensatory capabilities of the patient, the patient's overall clinical condition, and the potential harm caused by alkali administration. Sodium bicarbonate and other comparable solutions are usually unnecessary with adequate carbohydrate and fluid replacement.
Alkalinizing agents
These agents are rarely used for the management of severe metabolic acidosis.
Sodium bicarbonate (Neut)
Bicarbonate therapy should be reserved for patients with severe life-threatening acidosis unresponsive to fluid resuscitation. Severe complications such as volume overload, hypernatremia, hyperosmolality, and paradoxical CSF acidosis can arise from bicarbonate administration. If bicarbonate therapy is initiated, do not attempt to fully correct the serum pH or bicarbonate level. Sodium bicarbonate should rarely be given as rapid bolus; instead, it should be added to the patient's IV fluid. Administration of bicarbonate in the presence of metabolic acidosis is a temporizing measure; place primary emphasis on correction of the underlying cause of the acidosis.
Adult
100mL of sodium bicarbonate 8.4% added to 1L of D5/0.45% NS or 150mL of sodium bicarbonate 8.4% added to 1L of D5W (sodium content of these mixtures approximates that of NS); administer IV
Pediatric
Initially, 1 mEq/kg IV, which is 1 mL/kg of 8.4% solution
None significant
Alkalosis; hypernatremia; severe pulmonary edema; hypocalcemia; abdominal pain of unknown etiology
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Rapid administration of this drug may result in paradoxical CSF acidosis, impaired oxygen delivery, hypokalemia, hypocalcemia, overshoot alkalosis, hypernatremia, or hyperosmolality
Vitamin supplementation
This is indicated to correct a thiamine deficiency.
Thiamine (Vitamin B-1)
Supplementation ensures adequate cofactor for maintenance of cellular aerobic respiration. CNS depletion of thiamine may result in Wernicke's encephalopathy. Chronic thiamine deficiency may cause heart failure. Thiamine is an important element of the treatment of AKA, but there is little evidence that patients without clinical signs of Wernicke's will have an acute decompensation when treated initially with dextrose alone. Although thiamine should always be administered, dextrose should not be withheld pending thiamine availability in patients without clinical signs of Wernicke's.
Adult
100 mg IV/IM q24h
Pediatric
Not established
None for this emergency
None for this emergency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); deaths have resulted from IV use; administer before or together with dextrose-containing fluids in suspected thiamine deficiency
More on Alcoholic Ketoacidosis |
| Overview: Alcoholic Ketoacidosis |
| Differential Diagnoses & Workup: Alcoholic Ketoacidosis |
 Treatment & Medication: Alcoholic Ketoacidosis |
| Follow-up: Alcoholic Ketoacidosis |
| References |
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Further Reading
Keywords
alcoholic ketoacidosis, AKA, alcoholic acidotic coma, alcohol withdrawal, acute metabolic acidosis, metabolic alkalosis, alcohol abuse, glycogen depletion, lipolysis, ketogenesis, ethanol consumption, ketonemia, alcoholism, chronic alcoholism, chronic alcohol abuse, ketones, substance abuse, ketosis, binge drinking, Wernicke encephalopathy, Wernicke's encephalopathy
